Blood Reviews RSS feed: Current Issue. This respected International journal, Blood Reviews , is a vital information resource, bringing together appraisals of clinical practice, and research from recognized experts. Specially commissioned articles from leading researchers and practitioners guarantee truly global coverage of all the sub-specialties of hematology. Blood Reviews publishes review articles covering the spectrum of clinical and laboratory haematological practice and research. Although most reviews are invited, the editors welcome suggestions from potential authors. They should first write a brief outline of an intended review and send this to Dr Trevor Baglin or to Dr Jacob M Rowe. http://www.bloodreviews.com/?rss=yesElsevier Inc.en © 2010 Elsevier Ltd. All rights reserved. Blood Reviews0268-960X244-5July 2010 © 2010 Elsevier Ltd. All rights reserved. healthpermissions@elsevier.comhttp://www.bloodreviews.com/article/PIIS0268960X10000275/abstract?rss=yesAbstract: Drug-induced immune hemolytic anemia (DIIHA) is rare; it can be mild or associated with acute severe hemolytic anemia (HA) and death. About 125 drugs have been implicated as the cause. The HA can be caused by drug-independent antibodies that are indistinguishable, in vitro and in vivo, from autoantibodies causing idiopathic warm type autoimmune hemolytic anemia (AIHA). More commonly, the antibodies are drug-dependent (i.e., will only react in vitro in the presence of the drug). The most common drugs to cause DIIHA are anti-microbials (e.g., cefotetan, ceftriaxone and piperacillin), which are associated with drug-dependent antibodies. The most common drug to cause AIHA is fludarabine. Finding out which drug is causing the problem and stopping that drug is the first approach to therapy. It is not easy to identify the drug interactions accurately in vitro; laboratories specializing in this area can be of great help.Immune hemolytic anemia associated with drug therapyGeorge Garratty10.1016/j.blre.2010.06.004Blood Reviews 24, 4 (2010)2010-07-22Blood Reviews2010-07-22244-5S0268-960X(10)X0004-2143150http://www.bloodreviews.com/article/PIIS0268960X10000263/abstract?rss=yesAbstract: Anticoagulation in children is problematic for many reasons, related to the patient population as well as the anticoagulant drugs themselves. This paper describes the multitude of reasons why providing anticoagulation therapy in children is different from anticoagulation therapy in adults, and hence why dedicated paediatric anticoagulant services are the ideal structure to provide this service. The paper then describes the three most common anticoagulants used in children, and details specifically what is and is not known about them in the paediatric population. Finally the paper addresses the issue of how best to introduce newer anticoagulant drugs into the paediatric population. There remains much research to be done in this field, in the meantime clinicians need to carefully consider the evidence available to them and manage each individual patient accordingly.Anticoagulation in neonates and children: Pitfalls and dilemmasPaul Monagle, Fiona Newall, Janine Campbell10.1016/j.blre.2010.06.003Blood Reviews 24, 4 (2010)2010-07-21Blood Reviews2010-07-21244-5S0268-960X(10)X0004-2151162http://www.bloodreviews.com/article/PIIS0268960X10000251/abstract?rss=yesAbstract: Immunoglobulin E (IgE) is a key mediator of anti-parasitic and anti-tumour immunity. However it is also a critical component of atopic and autoimmune diseases, and elevated serum IgE levels are a common indicator of immune dysregulation. In this review we survey the literature on genetic associations of elevated IgE in humans and mice. We find that defects in a limited number of pathways explain the majority of gene associations with IgE. Commonly, elevated IgE is associated with defects in Th bias and B cell class switching, severe T cell tolerance defects and defects in immunity at the host–environment interface. These genetic data demonstrate the mechanisms of control over IgE production and the manner in which they can be circumvented.Understanding the genetic regulation of IgE productionJohn Altin, Chong Shen, Adrian Liston10.1016/j.blre.2010.06.002Blood Reviews 24, 4 (2010)2010-07-16Blood Reviews2010-07-16244-5S0268-960X(10)X0004-2163169http://www.bloodreviews.com/article/PIIS0268960X1000024X/abstract?rss=yesAbstract: Whether to continue oral anticoagulant therapy indefinitely after completing 3 to 6months of oral anticoagulant therapy for “unprovoked” venous thromboembolism (VTE), is one of the most important unanswered questions in VTE management. This long-term decision should be based on balancing the long-term mortality risk from recurrent VTE, largely preventable with oral anticoagulant therapy, against the long-term mortality risk of major bleeding, the principle complication of oral anticoagulant therapy. There exist important knowledge gaps in estimating the long-term mortality risk of recurrent VTE in patients with unprovoked VTE who discontinue therapy and the long-term mortality risk from major bleeding in those who continue oral anticoagulant therapy. These knowledge gaps, reviewed herein, are the source of uncertainty for patients and health care providers wrestling with this important question. One promising solution is recurrent VTE risk stratification where unprovoked VTE patients are categorised as low or high risk for recurrent VTE and clinical decision making is less ambiguous and ultimately will likely lead to better outcomes.Unprovoked Venous Thromboembolism: Short term or Indefinite Anticoagulation? Balancing Long-Term Risk and BenefitM. Rodger, M. Carrier, E. Gandara, G. Le Gal10.1016/j.blre.2010.06.001Blood Reviews 24, 4 (2010)2010-07-15Blood Reviews2010-07-15244-5S0268-960X(10)X0004-2171178http://www.bloodreviews.com/article/PIIS0268960X10000238/abstract?rss=yesAbstract: Thrombopoietin (TPO) is the key cytokine involved in thrombopoiesis, and is the endogenous ligand for the thrombopoietin receptor that is expressed on the surface of platelets, megakaryocytes, and megakaryocytic precursors.First-generation thrombopoietic agents were recombinant forms of human TPO, and their development was discontinued after prolonged thrombocytopenia due to neutralizing auto-antibodies cross-reacting with endogenous TPO was observed. Second-generation thrombopoiesis-stimulating molecules are now available, which have unique pharmacological properties and no sequence homology to endogenous TPO. Two of these new agents, romiplostim and eltrombopag, have already completed phase III trials in primary immune thrombocytopenia and have been granted marketing authorization for use in this disease. Phase II and III trials with these novel drugs are ongoing in other conditions characterized by thrombocytopenia, such as chemotherapy, chronic liver disease, and the myelodysplastic syndromes. Most of the other second-generation thrombopoietic growth factors are in early phase clinical development.Thrombopoietic agentsRoberto Stasi, Jenny Bosworth, Elizabeth Rhodes, Muriel S. Shannon, Fenella Willis, Edward C. Gordon-Smith10.1016/j.blre.2010.04.002Blood Reviews 24, 4 (2010)2010-05-24Blood Reviews2010-05-24244-5S0268-960X(10)X0004-2179190http://www.bloodreviews.com/article/PIIS0268960X10000226/abstract?rss=yesAbstract: Over the last 17years, clinical trials conducted worldwide have demonstrated the efficacy of arsenic trioxide (As2O3) in the treatment of relapsed acute promyelocytic leukemia (APL). Currently, the role of As2O3 in front-line therapy is under investigation. Recent trials in the US have demonstrated that the addition of As2O3 to standard treatment regimens improves survival outcomes in patients with APL and may allow a reduction in cytotoxic chemotherapy exposure. As2O3 has also shown efficacy in other malignancies, particularly multiple myeloma and myelodysplastic syndromes. Therapeutic doses of As2O3 are well tolerated, with no evidence of long-term toxicity. Adverse events include APL differentiation syndrome, electrocardiographic abnormalities, and mild elevations in liver enzymes. This review highlights trials investigating the role of As2O3 in induction and consolidation for newly diagnosed APL, as well as its role in other hematologic malignancies. The chemistry, mechanisms of action, and clinical side effects of As2O3 are also discussed.Arsenic trioxide — An old drug rediscoveredAshkan Emadi, Steven D. Gore10.1016/j.blre.2010.04.001Blood Reviews 24, 4 (2010)2010-05-17Blood Reviews2010-05-17244-5S0268-960X(10)X0004-2191199http://www.bloodreviews.com/article/PIIS0268960X10000287/abstract?rss=yesThe authors would like to correct the omission of a reference in their discussion of the genetic interaction between Sdo1 and Tif6 in yeast. This work was published by Menne TF, Goyenechea B, Sanchez-Puig N, Wong, C. C., Tonkin, L. M., Ancliff, P. J., Brost, R. L., Costanzo, M., Boone, C., Warren, A. J.. The Shwachman–Bodian–Diamond syndrome protein mediates translational activation of ribosomes in yeast. Nat Genet. 2007;39:486–495.Corrigendum to “Pathophysiology and management of inherited bone marrow failure syndromes” [Blood Reviews 24 (2010) 101–122]Akiko Shimamura, Blanche P. Alter10.1016/j.blre.2010.06.005Blood Reviews 24, 4 (2010)2010-07-26Blood Reviews2010-07-26244-5S0268-960X(10)X0004-2Corrigendum201201